ReviewDiabetes2021
Modulation of Leukocytes of the Innate Arm of the Immune System as a Potential Approach to Prevent the Onset and Progression of Type 1 Diabetes.
Review in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Age-independent immune subtypes in type 1 diabetes exhibit distinct post-onset progression rates and immunotherapeutic responses.Diabetologia · 2026Article
- Nanoparticle-neutrophils interactions for autoimmune regulation.Advanced drug delivery reviews · 2024Review
- CD56 Expression in Spleen Tissue Pathology and Its Implications in the Development of Type 1 Diabetes: Insights from Diabetic Rat Models.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2024Article
- Circulating platelet-neutrophil aggregates characterize the development of type 1 diabetes in humans and NOD mice.JCI insight · 2022Article
- The Contribution of Neutrophils and NETs to the Development of Type 1 Diabetes.Frontiers in immunology · 2022Review
- Gut microbiome and metabolic activity in type 1 diabetes: An analysis based on the presence of GADA.Frontiers in endocrinology · 2022Article
- Metformin to decrease COVID-19 severity and mortality: Molecular mechanisms and therapeutic potential.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Type I IFN-Driven Immune Cell Dysregulation in Rat Autoimmune Diabetes.ImmunoHorizons · 2021Article
- Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes.Frontiers in pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes (T1D) is characterized by insulin deficiency resulting from the selective destruction of pancreatic β-cells by self-reactive T cells. Recent evidence demonstrates that innate immune responses substantially contribute to the pathogenesis of T1D, as they represent a first line of response to danger/damage signals. Here we discuss evidence on how, in a relapsing-remitting pattern, pancreas remodeling, diet, microbiota, gut permeability, and viral/bacterial infections induce the accumulation of leukocytes of the innate arm of the immune system throughout the pancreas. The subsequent acquisition and presentation of endocrine and exocrine antigens to the adaptive arm of the immune system results in a chronic progression of pancreatic damage. This process provides for the generation of self-reactive T-cell responses; however, the relative weight that genetic and environmental factors have on the etiopathogenesis of T1D is endotype imprinted and patient specific. With this Perspectives in Diabetes, our goal is to encourage the scientific community to rethink mechanisms underlying T1D pathogenesis and to consider therapeutic approaches that focus on these processes in intervention trials within new-onset disease as well as in efforts seeking the disorder's prevention in individuals at high risk.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.